3 ms·

Type 1 Diabetes is due to the total loss of insulin-producing pancreatic beta cells. The loss is a result of autoimmune destruction. This brings up the followin

Type 1 Diabetes is due to the total loss of insulin-producing pancreatic beta cells. The loss is a result of autoimmune destruction. This brings up the following questions: 1. Will the transplanted cells produce insulin in a human host? 2. Will the transplanted cells be targeted by the host's immune system and be destroyed just like the original beta cells? 3. Will the beta cells produce insulin in response to the same regulatory pathways as original system? One major problem with self-injected insulin administration is overdose. Those are the questions I'd look to answer in the future.

BlakePetersen 12y ago
I am Type 1 Diabetic. I have done some research, but am by no means an expert. 1. Yes 2. No. "Melton said that the device Anderson and his colleagues at Massachusetts Institute of Technology are testing has thus far protected beta cells implanted in mice from immune attack for many months. “They are still producing insulin,” Melton said." There are two breakthroughs. The mass production AND the ability of the device to protect the cells from destruction. 3. Yes. It reacts ideally in pretty much all scenarios. When you eat, it produces insulin. When you fast, it doesn't lower you into hypoglycemia. When you're sick (like a cold) it regulates insulin as it should, as your body needs more or less as your insulin sensitivity is off. This is definitely HUGE!
- possibilistic 12y ago
  The mice used in the protocol were SCID mice [1]. They do not produce B or T lymphocytes (and thus no Ig either). Pretty much no adaptive immune system to speak of. These are a mainstay of murine study. The discussion section referred to the existing technique of islet transplantation [2]. This is sourced from cadaver tissue, and as such requires immunosuppressants. Obviously needed to counteract host v. graft, but I wouldn't be surprised if it masked the autoimmune recognition. The discussion section alludes to several future hurdles: gene expression differences from primary cell sources, transduction response, local tissue effects (need for tissue engineering), need to produce alpha, gamma, delta, and epsilon cells (alpha and gamma may be important to precise beta function), questions regarding long-term maintenance of phenotype, ... Nevertheless, this is very exciting! Stem cell researchers are truly hackers in every sense. The results here aren't only applicable to diabetes research, either. Patients aren't the only ones that need these cells. [1] http://en.wikipedia.org/wiki/Severe_combined_immunodeficiency_(non-human) http://en.wikipedia.org/wiki/Severe_combined_immunodeficienc... [2] http://en.wikipedia.org/wiki/Islet_cell_transplantation http://en.wikipedia.org/wiki/Islet_cell_transplantation

BlakePetersen 12y ago

I am Type 1 Diabetic. I have done some research, but am by no means an expert. 1. Yes 2. No. "Melton said that the device Anderson and his colleagues at Massachusetts Institute of Technology are testing has thus far protected beta cells implanted in mice from immune attack for many months. “They are still producing insulin,” Melton said." There are two breakthroughs. The mass production AND the ability of the device to protect the cells from destruction. 3. Yes. It reacts ideally in pretty much all scenarios. When you eat, it produces insulin. When you fast, it doesn't lower you into hypoglycemia. When you're sick (like a cold) it regulates insulin as it should, as your body needs more or less as your insulin sensitivity is off. This is definitely HUGE!

possibilistic 12y ago
The mice used in the protocol were SCID mice [1]. They do not produce B or T lymphocytes (and thus no Ig either). Pretty much no adaptive immune system to speak of. These are a mainstay of murine study. The discussion section referred to the existing technique of islet transplantation [2]. This is sourced from cadaver tissue, and as such requires immunosuppressants. Obviously needed to counteract host v. graft, but I wouldn't be surprised if it masked the autoimmune recognition. The discussion section alludes to several future hurdles: gene expression differences from primary cell sources, transduction response, local tissue effects (need for tissue engineering), need to produce alpha, gamma, delta, and epsilon cells (alpha and gamma may be important to precise beta function), questions regarding long-term maintenance of phenotype, ... Nevertheless, this is very exciting! Stem cell researchers are truly hackers in every sense. The results here aren't only applicable to diabetes research, either. Patients aren't the only ones that need these cells. [1] http://en.wikipedia.org/wiki/Severe_combined_immunodeficiency_(non-human) http://en.wikipedia.org/wiki/Severe_combined_immunodeficienc... [2] http://en.wikipedia.org/wiki/Islet_cell_transplantation http://en.wikipedia.org/wiki/Islet_cell_transplantation